Epidemiological analysis of influenza virus type A in hospitalized children with respiratory tract infection in Suzhou area from 2006 to 2015 / 中华实验和临床病毒学杂志

Objective@#To analyze the epidemiological characteristics of influenza virus type A (FluA) in children with respiratory tract infection, and to provide scientific basis for clinical diagnosis and treatment.@*Methods@#Sputum specimens of 35 529 cases of hospitalized children with respiratory tract diseases from January 2006 to December 2015 in Suzhou were collected. FluA was detected by direct immunofluorescence and the FluA detection result was analyzed. Groups were compared with chi-square test.@*Results@#The FluA infection rate was 1.60% in 35 529 children. The FluA infection rate of boys was 1.58%, and the rate of girls was 1.63%. There was no obvious statistically significant difference in sex (χ2=0.139, P=0.709). The FluA infection rates of children at the age of less than 1 year, less than 3 years, less than 7 years and older than 7 years respectively were 1.12%, 2.49%, 1.78%, and 1.24%; there was significant differences among these result (χ2=75.401, P=0.000). The FluA infection rates in spring, summer, autumn and winter respectively were 0.88%, 1.44%, 1.32%, 2.70%. The rates in four seasons had significant difference (χ2=105.432, P=0.000). The FluA infection rate was the highest in winter and the lowest in spring. The FluA infection rate was 6.55% in the autumn of 2008, which was the highest in the recent ten years.@*Conclusions@#FluA is one of the important pathogens of respiratory tract infection in children in Suzhou area. The infection rate of infant is higher and the epidemic peak is in winter. The FluA infection has obvious epidemic season and year. The FluA infection rates in Suzhou area are 0.64%-3.49%, and there was no outbreak in the recent ten years.

Etiology and Clinical Features of Viral Lower-respiratory Tract Infections in Children in Winter, 2003 / 소아과

PURPOSE: This study was performed to characterize the etiology and clinical features of acute viral lower-respiratory tract infections (LRI). METHODS: Etiologic agents and clinical features of acute viral LRI were studied from October. 2003 through March. 2004 in hospitalized children with LRI (253 cases) at Samsung Cheil Hospital. The viruses were identified by indirect immunofluorescent method. Medical records of patients with proven viral LRI were reviewed retrospectively. RESULTS: Ninety two cases (36.4%) were confirmed as viral infections. The identified pathogens were respiratory syncytial virus (RSV, 76.0%), adenovirus (ADV, 12.0%), influenza virus type A (INFA, 9.8 %), influenza virus type B (INFB, 1.1%) and parainfluenza virus (PIV, 1.1%). Eight four point eight% of patients were younger than 2 years of age. Clinical diagnosis of LRI were pneumonia (56.5%), bronchiolitis (35.9%), tracheobronchitis (4.3%) and croup (3.3%). The clinical symptoms and signs were cough (98.8%), rhinorrhea (82.6%), fever (70.7%), rale (67.4%), wheezing (29.3%), chest retraction (28.3%) and cyanosis (4.3%). The severe respiratory symptoms and signs were more common in RSV-infected patients, even cyanosis could be observed. Seventeen point four percent of patient had fever of 38.5degrees C or higher and their most common etiologic agent was INFA (66.7%). Twenty three point nine percent had fever more than 5 days and common etiologic agent was INFA (77.8%). The elevated WBC count (> 14x10 (3)/microliter) was in 14.1%, and common etiologic agents were INFA (22.2%) and ADV (18.2%). C-reactive protein (CRP > 4.0 mg/dL) was increased in 13.0%, and common in ADV (63.6 %). Increased aspartate aminotransferase (AST)/alanine aminotransferase (ALT) was detected in 10.9%, and the most common etiologic agent was RSV (12.9%). CONCLUSION: The common agents of acute viral LRI were RSV, ADV and INF, respectively. Because the etiologic agents present variable clinical features, it may be helpful to treat and to evaluate acute viral LRI that we should understand their etiologic variability.

Biosynthesis and function verification of short hairpin RNA targeting to Influenza A virus / 第三军医大学学报

Objective To investigate the inhibitive effects of biosynthesized short hairpin RNA(shRNA)on the duplication of Influenza A virus(IAV)in human bronchial epithelium(HBE)cells.Methods NP-shRNA and PA-shRNA targeting to the highly conservative sequences of IAV nucleoprotein(NP)and acidic RNA polymerase(PA)were designed and biosynthesized by in vitro transcription,and then were inserted into the plasmid pGenSil-1.After sequencing analysis,the recombinant plasmids NP-shRNA and/or PA-shRNA were transduced into HBE cells followed by infected with IAV A/PR/8/34 H1N1(A/PR8)virus.The cytopathogenic effect(CPE)of the HBE cells,hemagglutination assay(HA)and 50% tissue culture infective dose(TCID50)titer of A/PR8 in the culture supernatants were determined respectively.The mRNA and protein expressions of NP and PA were detected by RT-PCR and Western blotting respectively,and the results were compared in order to evaluate the inhibitive efficiency of NP-shRNA and/or PA-shRNA to A/PR8 duplication in HBE cells.Results The content of NP-shRNA and PA-shRNA biosynthesized by in vitro transcription were respectively 59.4 nmol and 50.6 nmol in each 100 ?l.The purity was more than 2.0 and the sequences were verified to be correct after sequencing analysis.The CPE of HBE cells and the virus titer in the culture supernatants of cells transfected with NP-shRNA,PA-shRNA or NP-shRNA+PA-shRNA were markedly lower than those of the control groups.In 3 h after 1 TCID50 A/PR8 infection,the mRNA level of NP in NP-shRNA group,the mRNA level of PA in PA-shRNA group and those in NP-shRNA+PA-shRNA group were 41.7%,43.4%,68.5% and 73.7% respectively,lower than those of the control group.At 48 h after 1 TCID50 A/PR8 infection,NP synthesis were 92.3%,84.0% and 91.7% respectively of those of the control group.Conclusion Anti-IAV NP-shRNA and PA-shRNA are successfully prepared by in vitro transcription.Both of those markedly inhibit the reproduction of IAV A/PR8 and produce a favorable protective effect on HBE cells.